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PubMed1989

Atypical hyperplasia in prostates of 20 to 40 year old men.

One hundred prostates from 20 to 40 year old men obtained at necropsy were completely sectioned and studied microscopically. Atypical hyperplasia was found in 10 (20%) of 20-29 year old men and in 12 (24%) of 30-40 year old men. The prostates with atypical hyperplasia had similar weights as those without, and the atypical hyperplasia was most common in the lateral lobes of the prostate and near the apex. The atypical hyperplasias were (i) usually mild in degree rather than moderate or severe; (ii) almost equally divided between circumscribed and "infiltrating" lesions; (iii) usually occurred as multiple foci within the same prostate rather than as a single focus of atypical hyperplasia; and (iv) were not associated with inflammation. The finding that atypical hyperplasia is common in men between the ages of 20 and 40 years may be helpful in increasing the understanding of the histopathology of the prostate.

Adult↗

PubMedDate not supplied

Thrombogenicity and intimal hyperplasia after conventional and thermal balloon dilation in normal rabbit iliac arteries.

Acute occlusion and restenosis are the major complications of percutaneous transluminal coronary balloon angioplasty. Application of heat during balloon dilation was postulated to reduce these complications. We evaluated thrombogenicity and intimal hyperplasia of normal rabbit iliac arteries after conventional (37 degrees C) and thermal balloon dilation. Thermal dilation was performed with a radio-frequency-heated balloon, provided with three thermocouples attached to the inside of the balloon skin. In a previous in vitro study, thrombogenicity of human subendothelium was increased at 55 degrees C and greatly decreased at temperatures over 70 degrees C. Thermal balloon dilation was therefore performed at 55 and 90 degrees C in vivo. Rabbits survived 2 h for evaluation of platelet adhesion or either 3 or 8 weeks for intimal hyperplasia. Angiograms revealed no occlusions or thrombi after any procedure. Platelet adhesion was quantified on 20 scanning electron microscopic pictures per balloon dilation site and was expressed as the percentage of the luminal surface covered by platelets. Platelet adhesion was similar in all groups, although large thrombi were present in the 90 degrees C group. Intimal hyperplasia was measured morphometrically at regular intervals over the balloon site. After 3 weeks, the average intimal hyperplasia was significantly reduced in the 90 degrees C balloon dilation group, which was mainly due to the absence of intimal hyperplasia in the midpart of these segments. After 8 weeks, intimal hyperplasia was equal in all groups. Thus, in the applied model, platelet coverage was equal after conventional balloon angioplasty and after 55 and 90 degrees C balloon angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Activation and hyperplasia of gastrin and enterochromaffin-like cells in the stomach.

The stomach is rich in endocrine cells, most of which are still unidentified with respect to the peptide hormones they produce. The endocrine cell populations in the antrum usually differ from those in the oxyntic mucosa. Gastrin cells are found in the antrum and respond readily to stimuli from the gastric lumen, such as changes in the pH and the presence of food. In order to study the functional control of the antral gastrin cell, rats were subjected to different kinds of surgery. The serum gastrin concentrations in the various experimental groups were measured 8-10 weeks after the operations. Elevated antral pH raised the serum gastrin concentration. The combination of elevated antral pH and the passage of food over the pyloric glands produced gastrin cell hyperplasia. The operation that was most effective in inducing gastrin cell hyperplasia was removal of the acid-producing part of the stomach. Interestingly, gastrin cell hyperplasia was seen also after bilateral truncal vagotomy, indicating that an intact vagal innervation is not essential for the development of gastrin cell hyperplasia. Enterochromaffin-like (ECL) cells are endocrine/paracrine cells that are numerous in the acid-producing part of the stomach in many species. In the rat, they occur predominantly in the basal half of the oxyntic mucosa and produce and store histamine. The ECL cells have an unknown function and do not seem to respond to stimuli from the gastric lumen. They are activated by circulating gastrin and by vagal excitation. Gastrin mobilises histamine from these cells and activates the histamine-forming enzyme, histidine decarboxylase. Long-term hypergastrinaemia produces diffuse ECL cell hyperplasia, whereas hypogastrinaemia (following removal of the endogenous stores of gastrin by antrectomy) reduces the ECL cell number. Portacaval shunt brings about a marked increase in the number of ECL cells through an unknown mechanism. Also neuronal stimuli are important for the trophic control of the ECL cells. Studies of unilaterally vagotomised rats showed reduced weight and thickness of the oxyntic mucosa as well as a markedly reduced number of ECL cells on the denervated side. Gastric carcinoids in man are rare tumours predominantly made up of ECL cells. The incidence of such tumours is increased in patients with hypergastrinaemia (pernicious anaemia, Zollinger-Ellison syndrome). A diffuse ECL cell hyperplasia is a common finding in such patients, which is in keeping with the known gastrin sensitivity of the normal ECL cell in the rat.

Animals↗

PubMed2002

Importance of monocyte chemoattractant protein-1 pathway in neointimal hyperplasia after periarterial injury in mice and monkeys.

Neointimal hyperplasia is a major cause of restenosis after coronary intervention. Because vascular injury is now recognized to involve an inflammatory response, monocyte chemoattractant protein-1 (MCP-1) might be involved in underlying mechanisms of restenosis. In the present study, we demonstrate the important role of MCP-1 in neointimal hyperplasia after cuff-induced arterial injury. In the first set of experiments, placement of a nonconstricting cuff around the femoral artery of intact mice and monkeys resulted in inflammation in the early stages and subsequent neointimal hyperplasia at the late stages. We transfected with an N-terminal deletion mutant of the human MCP-1 gene into skeletal muscles to block MCP-1 activity in vivo. This mutant MCP-1 works as a dominant-negative inhibitor of MCP-1. This strategy inhibited early vascular inflammation (monocyte infiltration, increased expression of MCP-1, and inflammatory cytokines) and late neointimal hyperplasia. In the second set of experiments, the cuff-induced neointimal hyperplasia was found to be less in CCR2-deficient mice than in control CCR2(+/+) mice. The MCP-1/CCR2 pathway plays a central role in the pathogenesis of neointimal hyperplasia in cuffed femoral artery of mice and monkeys. Therefore, the MCP-1/CCR2 pathway can be a therapeutic target for human restenosis after coronary intervention.

Animals↗

PubMed1999

CD10/neutral endopeptidase inhibition augments pulmonary neuroendocrine cell hyperplasia in hamsters treated with diethylnitrosamine and hyperoxia.

In previous studies, we demonstrated that pulmonary neuroendocrine cell (PNEC) hyperplasia in hamsters treated with diethylnitrosamine (DEN) plus 65% hyperoxia (DEN/O2) reflects predominantly neuroendocrine cell differentiation. Several peptides implicated in non-neoplastic PNEC hyperplasia are hydrolyzed by CD10/neutral endopeptidase 24.11 (CD10/NEP), an enzyme known to downregulate neurogenic inflammation of the lung by modulating locally effective concentrations of multiple bioactive peptides. In fetal mice, we observed that CD10/NEP inhibition by SCH32615 potentiates cell proliferation and type II cell differentiation in the lung in utero. Further, CD10/NEP messenger RNA levels parallelled relative PNEC numbers in DEN/O2-treated hamster lung, suggesting that the enzyme might mediate spontaneous regression of PNEC hyperplasia. The goals of the present study were: (1) to determine whether CD10/NEP inhibition would alter the extent of PNEC hyperplasia occurring in these hamsters, and (2) to analyze cellular mechanisms potentially involved in altering numbers of PNECs in this model. We administered SCH32615 chronically to a subset of DEN/O2-treated hamsters. Immunostaining of lungs from the CD10/ NEP-inhibited subset demonstrated significant acceleration of the development of PNEC hyperplasia, increased PNEC proliferation, and diminished PNEC apoptosis as compared with animals receiving no SCH32615. These observations indicate that PNEC hyperplasia can occur as a result of multiple cellular processes, including increased neuroendocrine cell differentiation, proliferation, and survival. CD10/NEP modulates PNEC numbers primarily by promoting cell differentiation and proliferation during lung injury, probably via increasing the half-life of bioactive peptides in the lung.

Animals↗

PubMed1979

Comparison of spontaneous and experimentally induced canine prostatic hyperplasia.

Spontaneous prostatic hyperplasia in the beagle appears to progress with age from a glandular to a cystic histological appearance. Prostatic hyperplasia can be induced in young beagles with intact testes by treatment for 4 mo with either dihydrotestosterone or 5 alpha-androstane-3 alpha, 17 beta-diol, alone, or with either of these steroids in combination with 17 beta-estradiol. In contrast, the induction of prostatic hyperplasia in young castrated beagles, in which the gland had been allowed to involute for 1 mo, requires the administration of both 17 beta-estradiol and either 5 alpha-androstane-3 alpha, 17 beta-diol or dihydrotestosterone. Testosterone and 17 beta-estradiol, either singly or in combination, did not produce the hyperplastic condition in intact or castrated beagles. The experimentally induced prostatic hyperplasia is identical in pathology to the glandular hyperplasia that occurs naturally in the aging dog with intact testes. However, cystic hyperplasia was not produced by any of the treatments tested in young animals.

Androstane-3,17-diol↗

PubMed1980

Androgen- and estrogen-receptor content in spontaneous and experimentally induced canine prostatic hyperplasia.

To gain insight into the mechanism by which steroidal hormones influence the development of canine prostatic hyperplasia, nuclear and cytosolic androgen- and estrogen-receptor content, as measured under exchange conditions by the binding of [(3)H]R1881 (methyltrienolone) and [(3)H]estradiol, respectively, were quantitated in the prostates of purebred beagles of known age. In young dogs with spontaneously arising and experimentally induced (androstanediol plus estradiol treatment) prostatic hyperplasia, nuclear, but not cytosolic, prostatic androgen-receptor content was significantly greater than that determined in the normal prostates of age-matched dogs (3,452+/-222 and 4,035+/-274 fmol/mg DNA vs. 2,096+/-364 fmol/mg DNA, respectively). No differences were observed between the androgen-receptor content of the normal prostates of young dogs and the hyperplastic prostates of old dogs. The cytosolic and nuclear estrogen-receptor content of spontaneously arising prostatic hyperplasia in both young and old animals was similar to that found in normal prostates. The administration of estradiol plus androstanediol to castrate dogs significantly increased the prostatic nuclear androgen-receptor content over that found in dogs treated only with androstanediol. This estradiol-associated increase in nuclear androgen-receptor content was accompanied by the development of benign prostatic hyperplasia. Estradiol treatment of castrate dogs resulted in an increase in prostatic nuclear estrogen-receptor content, in the appearance of a putative prostatic cytosolic progesterone receptor, and in an alteration of the epithelium of the prostate to one characterized by squamous metaplasia. Treatment of castrate dogs with both estradiol and androstanediol resulted in a reduction in prostatic nuclear estrogen-receptor content, disappearance of the progesterone receptor, and loss of squamous metaplasia. An increase in nuclear androgen-receptor content, thus, appears to be an important event in the development of both spontaneously arising and experimentally induced canine prostatic hyperplasia. The mechanism of androgen-estrogen synergism in the experimental induction of canine benign prostatic hyperplasia may be explained by estradiol-mediated increases in nuclear androgen-receptor content. Because androstanediol blocked certain estradiol-mediated events within the prostate, a negative feedback mechanism may exist in which the response of the canine prostate to estrogens is modulated by rising levels of androgen.

Androstane-3,17-diol↗

PubMed1988

Gastric ECL-cell hyperplasia and carcinoids in rodents following chronic administration of H2-antagonists SK&F 93479 and oxmetidine and omeprazole.

The histamine H2-receptor antagonist SK&F 93479 induced gastric neuroendocrine (carcinoid) ECL-cell tumor formation in 6/34 male and 8/37 female rats treated for 22-24 months at 1,000 mg/kg/day po. Focal ECL-cell hyperplasia was present in 21/34 males and 15/37 females, with local infiltration through the muscularis mucosae in half these cases. No focal hyperplasias or carcinoids were present after 200 mg/kg/day po treatment. Investigative studies showed evidence for marked and sustained hypergastrinemia increasing on chronic dosing which was capable of restoring gastric acid secretion and pH to near control values. Using morphometric analysis of immunoperoxidase anti-chromogranin A stained sections, a dose-related and time-dependent neuroendocrine ECL-cell hyperplasia was correlated with the sustained elevated hypergastrinemia. A 21-month mouse oncogenicity study showed no focal neuroendocrine cell hyperplasia or carcinoid tumor induction, but a diffuse neuroendocrine cell hyperplasia and an increase in multifocal glandular hyperplasia of the oxyntic mucosa was observed in mice treated with 1,000 mg/kg SK&F 93479 po. The morphological changes observed in both rat and mouse were considered to be secondary to the hypergastrinemia resulting from the pharmacological suppression of gastric acid secretion by SK&F 93479. These changes were also observed to a more marked degree following omeprazole treatment and were only slight following oxmetidine treatment in the rat.

Animals↗

PubMed2005

Atypical adenomatous hyperplasia (adenosis) of the prostate: DNA ploidy analysis and immunophenotype.

Atypical adenomatous hyperplasia (AAH) of the prostate is a microscopic proliferation of small acini that may be mistaken for adenocarcinoma. Although some data suggest that AAH is associated with adenocarcinoma arising in the transition zone, the clinical significance of this lesion is uncertain. Therefore we studied the DNA ploidy pattern and immunophenotype of AAH as compared with nodular hyperplasia and well-differentiated adenocarcinoma in 23 formalin-fixed, paraffin-embedded, whole-mounted retropubic prostatectomies. Representative sections were immunostained for keratin 34beta-E12, chromogranin, bcl-2, c-erbB-2, ki67-MIB1, and factor VIII (microvessel density). DNA ploidy was determined by image analysis and Feulgen-stained sections. There were rare scattered immunoreactive cells for chromogranin, bcl-2, and c-erbB-2 in nodular hyperplasia and AAH (mainly in the basal cell compartment) and in carcinoma. The ki67-MIB1 labeling index was different between nodular hyperplasia and AAH (p<0.001) and carcinoma (p=0.003) but not between AAH and carcinoma (p=0.203). Microvessel density was different between AAH and carcinoma (p=0.001) but not between nodular hyperplasia and AAH (p=0.105) or carcinoma (p=0.0820). All foci of nodular hyperplasia, AAH, and carcinoma were diploid. Ploidy status and our selected panel of antibodies did not discriminate among these 3 entities reliably.

Adenocarcinoma↗

PubMed2003

Inter-examiner reliability of the diagnosis of cervical pillar hyperplasia (CPH) and the correlation between CPH and spinal degenerative joint disease (DJD).

BACKGROUND: Cervical pillar hyperplasia (CPH) is a recently described phenomenon of unknown aetiology. Its clinical importance is poorly understood at the present time; therefore, the objective of this study was to determine (1) the inter-examiner reliability of detecting CPH and (2) if there is a clinically important correlation (r > 0.4) between the number of cervical spine levels showing signs of degenerative joint disease (DJD) and CPH. METHODS: The sample consisted of 320 radiographs of human male and female subjects who ranged from 40 to 79 years of age. The inter-examiner reliability of assessing the presence/absence of pillar hyperplasia was evaluated on 50 neutral lateral radiographs by two examiners using line drawings and it was quantified using the kappa coefficient of concordance. To determine the presence/absence of hyperplastic pillars as well as the presence/absence of DJD at each intervertebral disc and zygapophysial joint, 320 AP open mouth, AP lower cervical and neutral lateral radiographs were then examined. The unpaired t-test at the 5% level of significance was performed to test for a statistically significant difference between the number of levels affected by DJD in patients with and without hyperplasia. The Spearman's rho at the 5% level of significance was performed to quantify the correlation between DJD and age. RESULTS: The inter-examiner reliability of detecting cervical pillar hyperplasia was moderate with a kappa coefficient of 0.51. The unpaired t-test indicated that there was no statistically significant difference (p > 0.05) between the presence/absence of cervical pillar hyperplasia and the number of levels affected by DJD in an age-matched population, regardless of whether all elements were considered together, or the discs and facets were analyzed separately. A Spearman correlation rank of 0.67 (p < 0.05) suggested a moderately strong correlation between the number of elements (i.e. discs/facets) affected, and the age of the individual. CONCLUSION: Cervical pillar hyperplasia is a reasonable concept that requires further research. Its evaluation is easy to learn and acceptably reliable. Previous research has suggested that CPH may affect the cervical lordosis, and therefore, alter biomechanics which may result in premature DJD. This current study, however, indicates that, globally, CPH does not appear to be related to the development of DJD.

Adult↗

PubMed2001

Germline RET 634 mutation positive MEN 2A-related C-cell hyperplasias have genetic features consistent with intraepithelial neoplasia.

C-cell hyperplasias are normally multifocal in multiple endocrine neoplasia type 2A. We compared clonality, microsatellite pattern of tumor suppressor genes, and cellular kinetics of C-cell hyperplasia foci in each thyroid lobe. We selected 11 females from multiple endocrine neoplasia type 2A kindred treated with thyroidectomy due to hypercalcitoninemia. C-cell hyperplasia foci were microdissected for DNA extraction to analyze the methylation pattern of androgen receptor alleles and microsatellite regions (TP53, RB1, WT1, and NF1). Consecutive sections were selected for MIB-1, pRB1, p53, Mdm-2, and p21WAF1 immunostaining, DNA content analysis, and in situ end labeling. Appropriate tissue controls were run. Only two patients had medullary thyroid carcinoma foci. Nine informative C-cell hyperplasia patients showed germline point mutation in RET, eight of them with the same androgen receptor allele preferentially methylated in both lobes. C-cell hyperplasia foci showed heterogeneous DNA deletions revealed by loss of heterozygosity of TP53 (12 of 20), RB1 (6 of 14), and WT1 (4 of 20) and hypodiploid G0/G1 cells (14 of 20), low cellular turnover (MIB-1 index 4.5%, in situ end labeling index 0.03%), and significantly high nuclear area to DNA index ratio. MEN 2A (germline point mutation in RET codon 634) C-cell hyperplasias are monoclonal and genetically heterogeneous and show down-regulated apoptosis, findings consistent with an intraepithelial neoplasia. Concordant X-chromosome inactivation and interstitial gene deletions suggest clone expansions of precursors occurring at a point in embryonic development before divergence of each thyroid lobe and may represent a paradigm for other germline mutations.

Amino Acid Substitution↗

PubMed2004

Effect of baicalein on experimental prostatic hyperplasia in rats and mice.

We determined the effect of baicalein on prostatic hyperplasia in experimental animal models. Prostatic hyperplasia was induced by testosterone propionate in mice and castrated rats and by transplantation of homologous strain fetal mice urogenital sinus in mice. With the histopathological examination, the efficacy of baicalein on prostate hyperplasia in experimental animals was evaluated by the activity of serum acid phosphatase (ACP) and the following norm of the prostate gland: the volume, wet weight, wet weight index, dry weight index, DNA contents and prostatic epithelial height and cavity diameter. Results showed that baicalein at doses of 260 and 130 mg/kg administrated intragastrically (i.g.) significantly inhibited prostatic hyperplasia in castrated rats induced by testosterone propionate compared with the negative control group (p<0.01). Baicalein at doses of 520 and 260 mg/kg (i.g.) also significantly inhibited prostatic hyperplasia in mice induced by transplantation of homologous strain fetal mouse urogenital sinus and by testosterone propionate (p<0.01). These results suggested that baicalein has an inhibitory effect on prostatic hyperplasia in experimental animals.

Acid Phosphatase↗

PubMed1997

Prevalence of amlodipine-related gingival hyperplasia.

Calcium channel blockers are known to contribute to gingival hyperplasia. The vast majority of reports discuss patients taking the drug nifedipine. During the past few years a newer calcium channel blocker, amlodipine, has been used with increasing frequency. To date, six cases have been published indicating that amlodipine may also promote gingival hyperplasia; however, no data have been reported regarding the prevalence of this phenomenon. The purpose of this study was to examine a large group of patients taking amlodipine and determine the prevalence of gingival hyperplasia. One hundred fifty dentate patients who had been taking amlodipine, 5 mg per day for at least 6 months, volunteered to undergo a screening examination for gingival hyperplasia. Mild hyperplasia (< 1/3 clinical crown) was found in five patients-a prevalence of 3.3%. This is significantly less (P < .001) than rates reported for patients taking nifedipine, and not significantly different from rates previously reported in control groups of cardiac patients not taking calcium channel blockers. The results from this group of patients indicated that amlodipine, 5 mg per day, did not induce gingival hyperplasia.

Adult↗

PubMed2002

Nifedipine induces gingival epithelial hyperplasia in rats through inhibition of apoptosis.

BACKGROUND: Nifedipine is used as a long-acting vasodilator; one of its side effects is gingival overgrowth, characterized by an accumulation of collagenous components within the gingival connective tissue and epithelial hyperplasia with elongated, branched rete pegs penetrating into the connective tissue. We investigated the effect of nifedipine on apoptosis of gingival keratinocytes of rats to elucidate the mechanism of nifedipine-induced gingival epithelial hyperplasia. METHODS: Twenty-day-old rats were fed a powdered diet containing or lacking nifedipine for 8 to 30 days. The mandibular gingiva and palatal mucosa were removed on days 8, 15, or 30, and epithelial thickness was examined by light microscopy. In situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay was used to examine apoptosis of keratinocytes in the epithelium. In addition, we examined the effects of nifedipine on proliferation of keratinocytes and epithelial cell life on day 8 by 5-bromo-2'-deoxyuridine (BrdU) staining. RESULTS: Microscopic examination showed gingival epithelial hyperplasia in nifedipine-treated rats after day 15. Apoptosis of gingival keratinocytes was seen to be inhibited in nifedipine-treated rats on day 8 and 15. Also, nifedipine did not induce an increase of keratinocyte proliferation activity in terms of the number of cells showing positive staining with BrdU. Prolongation of cell life by nifedipine was observed on day 8 in gingival epithelium through a delay of upward cell movement compared to controls. However, epithelial hyperplasia was not detected in palatal mucosa, and there were no significant differences in apoptotic rates of keratinocytes and cell life between nifedipine-treated rats and control rats. CONCLUSIONS: These results suggest that nifedipine induces epithelial hyperplasia in gingival overgrowth not by an increase in keratinocyte proliferation, but by prolongation of cell life through reduction of apoptosis before epithelial hyperplasia is detectable.

Animals↗

PubMed1993

Alfuzosin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in benign prostatic hyperplasia.

Alfuzosin, a new quinazoline derivative, acts as a selective and competitive antagonist of alpha 1-adrenoceptor-mediated contraction of prostatic, prostatic capsule, bladder base and proximal urethral smooth muscle, thereby reducing the tone of these structures. Consequently, urethral pressure and resistance, bladder outlet resistance, bladder instability and symptoms associated with benign prostatic hyperplasia are reduced. A limited range of clinical studies have shown oral alfuzosin to be more effective than placebo (in studies of < or = 6 months duration), to have sustained effects on long term administration (< or = 30 months), and to be comparable with the alpha 1-adrenoceptor antagonist prazosin, in the symptomatic treatment of benign prostatic hyperplasia. This is reflected in increases in urinary flow rate and decreases in symptom score and residual urinary volume. The most marked improvements occur in patients with severe pretreatment urinary flow abnormalities. Furthermore, preliminary results suggest a beneficial effect of alfuzosin on quality of life in patients with benign prostatic hyperplasia. The overall incidence of adverse effects appears similar to that with placebo, and the incidence of vasodilatory-related adverse effects appears lower than that with prazosin. The relative selectivity of alfuzosin for alpha 1-adrenoceptors in the genitourinary tract compared with receptors in the vasculature is a potential advantage over other alpha-adrenoceptor antagonists, including prazosin, as the symptoms of benign prostatic hyperplasia may be reduced by alfuzosin at doses that have minimal vasodilatory effects, thereby minimising postural hypotension and syncope. However, vasodilatory-related adverse effects are the most common adverse effects that occur with alfuzosin, and dose and first-dose hypotensive relationships, especially in the elderly, cannot be excluded at this stage in the clinical use of alfuzosin. The full potential of alfuzosin in the symptomatic treatment of benign prostatic hyperplasia will be clarified by further long term comparative studies (with large patient numbers) against placebo and other alpha 1-adrenoceptor antagonists. Nevertheless, oral alfuzosin 7.5 to 10 mg/day in divided doses appears to be a promising first-line agent for symptomatic treatment of noncomplicated mild to moderate benign prostatic hyperplasia in patients with a high dynamic component to their obstruction. In addition, alfuzosin offers an alternative to prostatectomy (the current 'gold standard') in patients who require surgery but are unfit for this treatment, and in patients requiring symptomatic relief while awaiting surgery.

Adrenergic alpha-Antagonists↗

PubMed1989

The detection of adrenal tumors and hyperplasia in patients with primary aldosteronism: comparison of scintigraphy, CT, and MR imaging.

We retrospectively reviewed the imaging studies in 17 proved cases of primary aldosteronism to determine the value of the procedures used to detect adrenal tumors or adrenal hyperplasia. The procedures included CT with 3-, 5-, and/or 10-mm-thick sections (17 patients), 131I-6 beta-iodomethyl-19-norcholesterol (NP-59) scintigraphy (16 patients), and MR imaging (six patients). Proof of the adrenal abnormality was established in cases of tumor (seven adenomas, one carcinoma) by surgery and in cases of adrenal hyperplasia by surgery (three cases); venous sampling (three cases); or combined clinical, biochemical, and imaging data (three cases). Both CT and scintigraphy detected six of the seven adenomas and the adrenal carcinoma (88%). Regarding hyperplasia, CT was correct in five of six and scintigraphy was correct in two of four cases proved by surgery or venous sampling. CT and NP-59 were concordant and suggested the diagnosis of hyperplasia in the remaining three cases without surgical or venous sampling proof. MR detected both cases of adenoma in which it was performed and showed evidence of hyperplasia in one of the four cases of hyperplasia in which it was performed. Although the number of patients in this series is too small to have much statistical power, these results suggest that CT and NP-59 scintigraphy are equivalent in the detection of adrenal abnormalities in patients with primary aldosteronism. The value of MR in the detection of small adrenal contour abnormalities was limited by slice thickness capabilities.

Adenoma↗

PubMed1992

Hematopoietic bone marrow hyperplasia: high prevalence on MR images of the knee in asymptomatic marathon runners.

In a prior study of marathon runners, we noticed that MR scans of the knee frequently showed hyperplasia of red (i.e., hematopoietic) bone marrow. Because the frequency of this finding in various populations is unknown, the purpose of this study was to determine the relative prevalences of hematopoietic bone marrow hyperplasia on MR examinations of the knees of healthy volunteers (n = 74), patients with symptoms of knee disorders (n = 54), and asymptomatic marathon runners (n = 23). The prevalence of hematopoietic bone marrow hyperplasia was 3% (2/74) for the healthy volunteers, 15% (8/54) for the patients, and 43% (10/23) for the marathon runners. The difference in prevalence between each of the three groups was statistically significant at p less than .05 in each case with hematopoietic bone marrow hyperplasia, the distal femur was the only area affected, while the epiphysis and proximal tibia were uninvolved. This pattern of affected bone marrow with hyperplasia of the hematopoietic marrow may be useful for the differential diagnosis. We postulate that the high prevalence of hematopoietic bone marrow hyperplasia in marathon runners may develop as a response to "sports anemia", which is commonly found in highly conditioned, aerobically trained athletes. Furthermore, this is considered to be a normal variant when found in the pattern described here.

Bone Marrow↗

PubMed2002

NIH conference. Future directions in the study and management of congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

Congenital adrenal hyperplasia describes a group of inherited autosomal recessive disorders characterized by an enzymatic defect in cortisol biosynthesis, compensatory increases in corticotropin secretion, and adrenocortical hyperplasia. 21-Hydroxylase deficiency is responsible for more than 95% of cases and is one of the most common known autosomal recessive disorders. The classic or severe type presents in the newborn period or early childhood with virilization and adrenal insufficiency, with or without salt loss; the mild or nonclassic form presents in late childhood or early adulthood with mild hyperandrogenism and is an important cause of masculinization and infertility in women. This wide range of phenotypic expression is mostly explained by genetic variation, although genotype-phenotype discrepancies have been described. Reproductive, metabolic, and other comorbid conditions, including risk for tumors, are currently under investigation in both forms of the disease. A high proportion of patients with adrenal incidentalomas may be homozygous or heterozygous for 21-hydroxylase deficiency. Women with congenital adrenal hyperplasia often develop the polycystic ovary syndrome. Ectopic adrenal rest tissue is often found in the testes of men with congenital adrenal hyperplasia; characteristic clinical and radiologic findings help differentiate this tissue from other tumors. Levels of corticotropin-releasing hormone are elevated in patients with depression and anxiety and are expected to be elevated in patients with congenital adrenal hyperplasia; it is unknown whether patients with 21-hydroxylase deficiency have an increased incidence of these psychiatric disorders. Abnormalities in both the structure and function of the adrenal medulla have been shown in patients with classic congenital adrenal hyperplasia, and the degree of adrenomedullary impairment may be a biomarker of disease severity. The 21-hydroxylase-deficient mouse has provided a useful model with which to examine disease mechanisms and test new therapeutic interventions in classic disease, including gene therapy. Treatment of this condition is intended to reduce excessive corticotropin secretion and replace both glucocorticoids and mineralocorticoids. However, clinical management is often complicated by inadequately treated hyperandrogenism, iatrogenic hypercortisolism, or both. New treatment approaches currently under investigation include combination therapy to block androgen action and inhibit estrogen production, and bilateral adrenalectomy in the most severely affected patients. Other approaches, which are in a preclinical stage of investigation, include treatment with a corticotropin-releasing hormone antagonist and gene therapy.

Adrenal Hyperplasia, Congenital↗